LAUSR

Acute myeloid leukemia (AML) is an invasive hematological malignancy of which the mechanism is still unknown. MicroRNAs (miRNAs) act as critical controllers of target gene expression at post-transcriptional level. MiR-1290 is found to abnormally express in multiple cancers, however, its role in AML is still unknown. In this study, the mRNA and protein expression levels of related genes were determined by quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and Western blot. Luciferase assay was used to verify the target genes of miR-1290. In addition, the cell proliferation, cell cycle and apoptosis of HL-60 and KG-1 cells were detected by Counting Kit-8 (CCK-8) and flow cytometry assay, respectively. Our results showed that the expression of miR-1290 was increased in AML in vivo and in vitro. Gain and loss of function experiments by transfection of miR-1290 mimics or miR-1290 inhibitors into HL-50 and KG-1 cells indicated that miR-1290 significantly promoted cell proliferation and inhibited cell apoptosis. Furthermore, Forkhead-box gene 1 (FOXG1) and Suppressor of cytokine signaling 3 (SOCS3) were verified to be the target genes of miR-1290. Overexpression of FOXG1 or SOCS3 inhibited cell proliferation and induced cell apoptosis in HL-50 and KG-1 cells. Moreover, knockdown of miR-1290 inhibited cell proliferation and promoted apoptosis, whereas these effects were reversed by silencing of FOXG1 or SOCS3 in HL-50 and KG-1 cells. In conclusion, miR- 1290 promoted proliferation and suppressed apoptosis in AML by targeting FOXG1 and SOCS3, which might provide a therapeutic target for AML.